European Surgical Research · Published 2025-08-26 · DOI 10.1159/000547900
Introduction: Pressure injuries (PIs) in patients with diabetes mellitus still impact patients’ health and place a heavy burden on healthcare systems. Stage I and stage II PIs are particularly prevalent among individuals with diabetes. Without timely and appropriate interventions, these injuries can progress to more severe stages, requiring prolonged recovery periods. Thus, the development of preclinical animal models that can mimic stage I or II PIs in diabetic patients is urgently needed to understand the mechanisms of injury formation and healing. Methods: In this study, magnets were used to compress the dorsal sides of mice for 2 h, 4 h, 8 h, or 16 h according to the ischemia-reperfusion principle, and the changes in compressed skin in diabetic (db/db) and non-diabetic (WT) mice were compared at different ischemia exposure times and cycle times. Results: After 2 h of ischemia, there was no significant injury in WT and db/db mice. On the third day following 4 h of ischemia, both db/db and WT mice exhibited characteristics resembling human stage II PIs, with damage primarily confined to the epidermis and upper dermis. Ischemia durations of 8 h and 16 h resulted in more severe full-thickness skin defects, including exposed subcutaneous adipose tissue and inward contraction of wound margins. After ischemia for 4 h and reperfusion for 24 h, the morphology of fibroblasts in the compressed skin area of db/db mice changed, and the expression of transforming growth factor (TGF)-β1 decreased significantly compared with those in WT mice. On day 5, epidermal-dermal separation and pronounced infiltration of inflammatory cells were evident in both groups. On day 10, db/db mice exhibited delayed wound closure, as well as impaired regeneration of the panniculus carnosus and dermis, with significantly decreased messenger RNA levels of vascular endothelial growth factor and HSP90. Conclusion: Ischemia lasting 4 h is the appropriate duration for generating stage II PIs in diabetic mice, which may be applicable to generate a reproducible model of stage II PI caused by ischemia-reperfusion injury. This model offers a valuable experimental tool for in-depth investigation of the pathogenesis of diabetic PIs and for the development of novel therapeutic strategies.
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